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Journal of Dental Health, Oral Disorders & Therapy
Malignant Neurocardiogenic Syncope: Recognition and
Management within the Dental Operatory
Case Report
Abstract
Neurocardiogenic Syncope is a form of Dysautonomia which commonly occurs
in children. It carries with it a potential for a range of responses from syncope to
cardiac arrest. Because of these recurring events, this condition has a significant
impact on their quality of life and causes them to alter daily routine living events.
This report details the symptoms, pathophysiology, malignant vasovagal syncope,
treatments, dental considerations, emergency management and highlights a
case report featuring a history of cardiac arrest in a patient with multiple dental
needs. The case outlines the efforts taken to avoid a repeat of complications from
this condition and the difficulties encountered when disagreements exist among
professionals. The perils of this condition are masked by their average appearance
at presentation and emphasize the importance of an accurate medical history.
Keywords: Neurocardiogenic syncope; Neuromediated faint; Vasovagal
syncope; Poatural orthostatic hypotension; Neurally mediated syncope; Primary
dysautonomia; Electrocardiogram; Autonomic nervous system; Head-up tilt table
test; Chronic fatigue syndrome
Abbreviations: NCS: Neuro Cardiogenic Syncope; WS:
Vasovagal Syncope; NMS: Neurally Mediated Syncope; ECG:
Electrocardiogram; HUTTT: Head-Up Tilt Table Test; CFS: Chronic
Fatigue Syndrome
Introduction
Dysautonomia is a general term for any medical condition
involving a dysregulation of the autonomic nervous system.
Although there are numerous types of dysautonomia, including
Shy-Drager syndrome and pure autonomic failure, a form
commonly found in pediatric patients is Neurocardiogenic
Syncope (NCS), which is also synonymous with vasovagal syncope
(WS) or neurally mediated syncope (NMS) [1]. The purpose of this
paper is to raise awareness of the primarily pediatric condition
and provide clinicians with a basic framework to recognize
evaluate and properly manage patients within the dental setting.
A case study is included that illustrates the difficulties associated
with treatment. Neurocardiogenic Syncope, or Vasovagal Syncope,
is the most common form of syncope comprising approximately
fifty percent of cases [2]. Syncope, otherwise known as “fainting,”
“passing out”, or “blacking out” is the most prevalent systemic
complication in dentistry [3,4]. Females have a higher incidence
than males, with a peak incidence within the 15-19 year-old
age group [5]. It is merely a symptom not a disease, which can
be defined by a rapid onset, transient loss of consciousness with
loss of postural control resulting from an insufficient supply of
oxygen to the brain [6]. Syncope is then classified according to the
underlying cause: neurological, psychiatric, metabolic and cardiac
[7]. Neurocardiogenic syncope is classified as having a nonarrhythmic, cardiac origin. Usually, neurocardiogenic syncope is
of a short duration with spontaneous recovery, although cases of
prolonged cardio inhibition leading to a systolic cardiac arrest
have been reported [6]. The significance of neurocardiogenic
syncope lies in the fact that the presentation and spectrum of the
condition vary immensely, ranging from patients having periodic
syncopal episodes to recurrent, non refractory syncopal events
Submit Manuscript | http://medcraveonline.com
Volume 2 Issue 3 - 2015
Stephanie Ferguson1 and Gary Badger2*
University of Texas School of Dentistry, USA
Department of Pediatric Dentistry, University of Texas School
of Dentistry, USA
1
2
*Corresponding author: Gary Badger, Chair, Department of
Pediatric Dentistry, University of Texas School of Dentistry,
7500 Cambridge St, Houston, TX 77054, USA, Tel: 713-4864141; Email:
Received: March 16, 2015 | Published: May 12, 2015
leading to a disabling condition with potential for cardiac arrest.
Symptoms
Neurocardiogenic Syncope may be abrupt or be associated
with a variety of prodromal symptoms including, but not limited
to lightheadedness, dizziness, abdominal discomfort, diaphoresis,
augmented hearing, visual changes, headaches, palpitations and
pallor [7-10]. If an adolescent has a syncopal event while driving,
participating in sports, or operating machinery, the result could be
trauma or even death. Therefore, many states suspend drivers and
pilots license after such events [6]. Often, prodromal symptoms
have specific triggers including pain, anxiety, dehydration and
phobic stress that usually occur while standing or sitting [11].
Many of the triggers can be initiated during routine dentistry. Due
to the highly variable nature of the condition, many patients with
recurrent syncope have profound impairment, in both physical
and psychosocial functioning. The quality of life of individuals that
suffer from recurrent neurocardiogenic syncope is diminished
due to debilitating symptoms, misdiagnosis, or ineffective
treatment. It is not uncommon for individuals with severe NCS
to miss substantial amounts of school, work and extracurricular
activities [12].
Pathophysiology
Although the exact mechanism of Neurocardiogenic Syncope
remains unclear, the most widely accepted mechanism of action
will be discussed. It is thought to occur due to an imbalance of
the autonomic nervous system. A disconnect occurs between
the autonomic nervous system and cardiovascular system.
Three separate phases occur. Initially, a stress occurs to the
cardiovascular system that reduces blood volume. During this
first phase, the reduction in blood volume caused by venous
pooling leads to an increase in sympathetic nervous system
activity, which subsequently increases heart rate and peripheral
resistance to maintain adequate blood pressure. The second
phase then begins; the vigorous contractions of a relatively empty
J Dent Health Oral Disord Ther 2015, 2(3): 00048
Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental
Operatory
left ventricle, causes activation of ventricular mechanoreceptors.
The activation of the vagal C fiber mechanoreceptors and other
baroreceptors cause the brain to receive conflicting information
on blood pressure. The brain then assumes the body to be in a
hypertensive crisis, which produces a compensatory mechanism
[13]. The third phase then occurs, resulting in a reflex bradycardia
(cardio inhibitory syncope) and/or an abnormal decrease in
blood pressure (vasodepressor syncope). These actions are the
end result of excessive parasympathetic activation combined with
sympathetic withdrawal [14].
Diagnosis
A diagnosis of neurocardiogenic syncope is obtained through
a series of evaluations including physical, neurological and
electrophysical, which includes an electrocardiogram (ECG).
If the ECG and cardiac testing results are normal, a head-up tilt
table test (HUTTT) may be ordered. Recently, debate has begun
regarding the efficacy of the once gold standard test for diagnosis
of neurocardiogenic syncope, the head-up tilt table test. Excessive
false-positive and false-negative results in children and adolescents
provide a source of debate amongst cardiologists [15,16]. The
first documented use of a tilt test was in the nineteenth century
[17]. Later, this tool was used by NASA to evaluate physiological
changes with change in posture [18]. Currently, the purpose of the
HUTTT is to assess the function of the autonomic nervous system
by eliminating the body’s compensatory mechanism of skeletal
muscle contraction, which preserves venous return [19,20].
After a period of fasting, individuals are placed on a tilt table
with a foot plate support. Restraining belts are placed over the
chest and thighs. The HUTTT begins after a 10 minute period
of supine observation. The individual is placed in a 70-degree
upright tilt and maintained for a period of 30-45 minutes,
during which time heart rate, rhythm and blood pressure are
monitored continually. If no symptoms or syncope occurs during
the time interval allotted, pharmacologic agents are used to
try to reproduce the triggering incident normally, just prior
to spontaneous vasovagal syncope, serum concentrations of
catecholamines increase. To simulate this catecholamine release,
isoproterenol, which stimulates B-adrenergic receptors, is infused
in an effort to provoke a syncopal event [21]. Other pharmacologic
agents used to provoke vasovagal syncope during a head-up tilt
table test include adenosine, nitroglycerin and edrophonium
[22-26]. In general, a HUTTT response is considered positive
for vasovagal syncope if syncopal symptoms are reproduced by
provoking hypotension or bradycardia, or both, as a result of the
procedure [27].
Although chronic fatigue syndrome (CFS) is an incompletely
understood disorder, there appears to be an association between
NCS and CFS. The profile of both NCS and CFS individuals are
similar in regards to gender, age and clinical presentation. When
using a HUTTT to evaluate patients with CFS, more than 60% have
abnormal blood pressure or heart rate responses with abrupt
hypotension or severe bradycardia and a subsequent decreased
level of consciousness [28-31]. Other studies have shown
CFS patients to benefit from combination therapy including
fludrocortisones along with increased sodium intake [29].
Malignant vasovagal syncope
As the severity and recurrence rates of vasovagal syncope
Copyright:
©2015 Ferguson et al.
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increases, a description of malignant vasovagal syncope is
assigned [32]. Individuals with malignant vasovagal syncope
have been reported to have episodes of prolonged asystole during
the HUTTT. One study suggested that systolic cardiac arrest may
occur in patients with this extreme form of vasovagal syncope
[33]. Another study of patients with vasovagal syncope found
that bradycardia and asystole occurred in up to 15% of patients
undergoing HUTTT, with the longest asystolic pause lasting 73
seconds [34,35]. There is limited knowledge on the prognosis of
malignant vasovagal syncope. Understanding the existence and
severity of this extreme form of vasovagal syncope is paramount.
Treatments
Education and non pharmacologic interventions are the firstline treatments of neurocardiogenic syncope. Both the patient
and family are educated as to the mechanism of vasovagal
syncope and individual triggers or situations that are to be
avoided. Patients are then taught to journal and recognize their
prodromal symptoms that could alert them to an impending
syncopal or near syncopal episode. Another cornerstone of nonpharmacologic treatment includes increasing blood volume by
adequate hydration, supplemental sodium and exercise. Eight to
ten sixteen ounce glasses of water and an increased sodium intake
by 200 mEq per day is required. Exercise recommendations
include combinations of aerobic and resistance training three
times per week for a duration of 30 minutes per session. Elastic
support stockings that provide 30-40 mm Hg counter pressure
prove useful in minimizing venous pooling [36]. Unfortunately,
non pharmacologic interventions are often inadequate and
pharmacologic management is required [37]. Neurocardiogenic
syncope can be mitigated by the use of mediators that will
increase blood pressure, such as midodrine. This medication
acts by stimulating alpha-1 adrenergic receptors to constrict
blood vessels and raise blood pressure within 30 minutes and
lasts approximately 4-5 hours [38]. It has proven to be the most
effective medication to prevent recurrent WS [39]. Low dose Bblockers including atenolol, metoprolol, propanol and nadolol
were once prescribed as first-line pharmacologic therapy for
WS. Recently, studies have shown little to no positive results
while implementing B-blockers [40]. Another medication,
fludrocortisones, which enhances the sensitivity of the vasculature
to circulating catecholamines and causes sodium retention, can be
used to bolster the circulatory fluid levels. A randomized placebocontrolled study in children revealed fludrocortisones to be
ineffective in preventing pre syncope and syncope [41].
Pacemaker placement is reserved for a select group of
NCS patients and its placement is controversial. After all non
pharmacologic and pharmacologic methods of treatment have
been exhausted without success, pacing may be considered.
Since a fall in blood pressure precedes bradycardia in most
people with neurocardiogenic syncope, pacing may be ineffective
in a majority of the patients. If NCS is caused by a large cardio
inhibitory component, dual chamber pacing may be effective in
reducing symptoms and preventing subsequent syncopal events
[42]. Specific indications for permanent pacing in patients with
NCS have been developed by the American Heart Association.
One indication for pacemaker placement includes patients with
malignant vasovagal syncope and asystole that is provoked in
electrophysiological studies [43].
Citation: Ferguson S, Badger G (2015) Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental Operatory. J Dent Health
Oral Disord Ther 2(3): 00048. DOI: 10.15406/jdhodt.2015.02.00048
Copyright:
©2015 Ferguson et al.
Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental
Operatory
Dental considerations and recommendations
Undergoing dental procedures evokes a range of bodily
responses that requires the autonomic nervous system to be
functioning properly at all times. Patients with a history of
neurocardiogenic syncope present with no immediately evident
pathognomonic clinical characteristics, but when treated without
precaution, a patient’s inability to respond to stress appropriately
can result in syncope or life threatening conditions including
asystolic cardiac arrest. To manage patients with neurocardiogenic
syncope, specific measures must be taken to ensure the patient’s
safety throughout treatment. Symptoms are typically exacerbated
by a multitude of triggers including emotional stress, pain and
dehydration. Dental procedures inherently produce these specific
triggers that could produce a syncopal event in a number of
individuals. First and foremost, a thorough medical history must
be obtained including examining triggers, last syncopal or near
syncope event, frequency and duration of symptoms, diagnostic
testing performed with results, medications and overall medical
management. During the inquiry regarding a syncopal event,
attempt to glean insight into three areas: the circumstances before
symptoms arise; prodromal symptoms; and how the patient felt
during the recovery period. Known risk factors for recurrent
neurocardiogenic syncope include female gender and the number
of previous syncopal spells [44]. Consultations from all specialists
including cardiologist and neurologist must be obtained prior
to beginning treatment. A collaborative effort must be made
when determining the safest treatment modality. If in-office
treatment is considered, precautions should be taken to prevent
a syncopal episode. Individual triggers should be identified and
avoided. Discourage morning appointments if possible, as blood
pressure is at its lowest in the early morning hours. Prior to the
appointment, request the patient to wear loose fit clothing. Also,
encourage the patient to maximize oral fluid intake and minimize
physical activity 24 hours prior to the dental appointment to
prevent dehydration [45]. During the appointment, attempt to
limit strong, noxious, sensory stimuli and avoid overheating
the dental operatory. Baseline vitals should be recorded
and continuous monitoring considered. Administering local
anesthetics with epinephrine should be considered carefully only
after a thorough pharmacological review. During administration
of local anesthetic, frequent aspirations are encouraged to prevent
inadvertent intravenous administration. Adequate anesthesia is
required to prevent pain from triggering a syncopal event [46]. At
the completion of treatment, raise the dental chair incrementally
and demand that the patient stay seated for 5 minutes to allow the
body to equilibrate to the change in posture. To manage the highly
anxious NCS dental patient, that may otherwise trigger a syncopal
event, nitrous oxide alone or in combination with sedation may
prove to be a valid treatment modality in specific mild forms
of NCS. Careful patient selection is critical. If a collaborative
decision to sedate the patient is made, fluid restrictions must
be minimized. Appropriate monitoring including an ECG and
emergency resuscitation must be available.
NCS patients would benefit from implementing a caries
prevention plan, due to the tendencies toward polypharmacy,
possible xerostomia, fatigue that could possibly contribute
to unsatisfactory oral hygiene regimens and a frequent, high
cariogenic diet. It would be prudent to consider increasing
the frequency of recall appointments and prescribing a highly
fluoridated dentifrice.
Emergency management
syncopal event
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neurocardiogenic
Essential ingredients to effective emergency management
in the event of neurocardiogenic syncope include protecting
and maintaining an open airway, proper positioning and closely
observing vitals. If a patient loses consciousness, the operator must
immediately cease treatment, remove foreign objects from the oral
cavity and activate predetermined office emergency management
protocol. Vital signs should be verified. Due to the variability of
presentation, severe cases may lead to neurocardiogenic shock,
resulting in a weak pulse, less than 60 beats/min. When the systolic
blood pressure is reduced to 50mm Hg, a pulse will be difficult to
palpate. After confirming hypotension, the patient should then be
placed in a Trendelenburg position. With the patients legs slightly
elevated, an increase in cerebral profusion will be achieved. During
the unconscious state, a patient’s airway is at risk of obstruction.
Techniques to ensure an open, patent airway include performing
a head tilt chin lift or jaw thrust. Additional airway management
includes administering supplemental oxygen at a flow rate of 6 L/
min [47]. The patient must be escorted upon dismissal and must
not drive an automobile [45]. If the episode is not self-limiting,
activate emergency medical services. Continue to monitor the
patient’s vitals, administer atropine intravenously and begin CPR
if necessary in the event of persistent, excessive vagal tone [48]. At
the conclusion of the event, a referral is mandated.
Description of Case
An eighteen year old female presented to the dental clinic
with a history significant for neurocardiogenic syncope and
adverse reactions to Propofol and Fosphenytoin. This patient’s
history indicated that during a colonoscopy approximately two
years prior to presentation for dental care, she experienced a
significant loss of blood pressure and was treated for bradycardia.
The patient was given epinephrine in a “rescue” dose and
arrested. After several days in a coma, she was revived and
recovered uneventfully. Because of this history and the need for
dental treatment on teeth that were having pain, it was decided
to proceed for treatment under general anesthesia. Consultations
were sent to cardiology, anesthesia and neurology. The patient
was taking Midodrine, Zoloft, Prilosec, Sinemet and Propranolol.
There was much disagreement among the specialists as to the
proper method of treatment; i.e. outpatient vs. inpatient. The
dentist performing the treatment did not want to proceed as an
outpatient due to the possibility of a recurrence of blood pressure
reduction and the possibility of instability. After nearly a year of
delay due to parent and physician delays, the case was admitted
to the hospital for treatment. On the morning of treatment, the
patient was hydrated with sterile saline using an IV and taken
to the operating room with the following treatment plan: The
patient received fifteen various restorations of anterior and
posterior teeth, many restored as a result of lesions occurring
during orthodontic treatment (Figures 1-7). The third molars
were removed by oral surgery as they were mesio-angular on
panographic radiographythe patient tolerated the procedures
well and was sent to recovery in improved condition. She was
seen in five days for a post-operative review with no sequalae
medically and a needed coverage of an open margin, dentally.
Citation: Ferguson S, Badger G (2015) Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental Operatory. J Dent Health
Oral Disord Ther 2(3): 00048. DOI: 10.15406/jdhodt.2015.02.00048
Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental
Operatory
Figure 1: Facial appearance.
Figure 5: Panoramic radiograph.
Figure 2: Maxilla.
Figure 6: Bitewing radiographs.
Figure 3: Mandible.
Figure 4: Dental occlusion.
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©2015 Ferguson et al.
4/6
Figure 7: Completed dental treatment.
Discussion
Patients with neurocardiogenic syncope present with
unsuspected underlying conditions that require significant
awareness. Without proper supervision, untoward events may
occur that can be life-threatening. A thorough medical history
is essential to prevent medical emergencies. Disagreement by
medical specialists as to treatment modalities may complicate
efficient treatments. Triggers for the patients included exertion,
pain, supine positioning and dehydration. The constant
irregularity of the symptoms interfered with daily activities and
quality of life. Maintaining hydration and using Midodrine to
control blood pressure as well as pressure apparel to the lower
extremities helped control symptoms. During the hospitalization,
the patient did not exhibit any of the suspected urgent situations
anticipated and recovered well.
Citation: Ferguson S, Badger G (2015) Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental Operatory. J Dent Health
Oral Disord Ther 2(3): 00048. DOI: 10.15406/jdhodt.2015.02.00048
Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental
Operatory
Conclusion
Neurocardiogenic syncope is an unsuspected medical
condition that requires overriding consideration before beginning
dental treatment. It is a condition that interferes with the daily
activities of living. Proper precautions are necessary to prevent
untoward events such as adequate hydration, postural positioning
and daily medications to control blood pressure. Dental treatment
recommendations for these patients must be well considered
before beginning patient treatment and prevention of physical
symptoms of dysautonomia must be strictly followed.
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Citation: Ferguson S, Badger G (2015) Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental Operatory. J Dent Health
Oral Disord Ther 2(3): 00048. DOI: 10.15406/jdhodt.2015.02.00048
Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental
Operatory
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Citation: Ferguson S, Badger G (2015) Malignant Neurocardiogenic Syncope: Recognition and Management within the Dental Operatory. J Dent Health
Oral Disord Ther 2(3): 00048. DOI: 10.15406/jdhodt.2015.02.00048